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. 2022 Mar 21;14:853180. doi: 10.3389/fnagi.2022.853180

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Copyright © 2022 Sayad, Najafi, Hussen, Abdullah, Movahedpour, Taheri and Hajiesmaeili.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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BACE1-AS promotes the synthesis of β-secretase in the brain of patients with AD. Amyloid plaques in the brain of patients with AD are linked to the illness. Plaques are formed by the successive breakdown of the APP via β-secretase (BACE1) and γ-secretase. In individuals with BACE1 deficiency, the mRNA is stabilized by binding to its antisense non-coding RNA (BACE1-AS). miRNAs, such as miR-34a-5p, miR-125b-5p, miR-15b, and miR-149, inhibit BACE1 expression, decrease amyloid accumulation, and ameliorate neuronal injury.